Components of flow-induced dilation in rat perfused coronary artery.

This study was undertaken to determine the endothelial factors involved in the flow-induced dilation of a rat perfused coronary artery. Segments of the right interventricular coronary artery were taken from 10-15-week-old male Wistar rats. Vessels were mounted in an arteriograph where internal diameter was continuously monitored while intraluminal pressure was controlled. Vessels were preconstricted with serotonin (10 mumol/L), and the dilation induced by flow (0-800 microliters/min) was quantified. This dilator effect was measured in control conditions, after incubation with L-NAME (100 mumol/L), with indomethacin (100 mumol/L), and after mechanical destruction of the endothelium (-E). Dilations were expressed as percentage of the serotonin-induced constriction, and wall shear stress tau due to the physical forces exerted on the wall of the vessel was calculated and expressed in dyn/cm2. In control conditions, raising the flow up to 800 microliters/min led to an increase in dilation (maximal dilation 63% +/- 4%) and in shear stress (maximal shear stress 76 +/- 4 dyn/cm2). With indomethacin, maximal dilation was 69% +/- 4% and maximal shear stress was 81 +/- 6 dyn/cm2. With L-NAME or after destruction of endothelium, dilation was greatly reduced (39% +/- 3% and 40% +/- 2%, respectively) whereas shear stress values were greatly increased (173 +/- 14 and 150 +/- 13 dyn/cm2, respectively). These results confirm the viability of this model for the study of flow-dependent dilation. This dilation seems to be greatly dependent on NO release. In contrast, results do not favor a significant involvement of prostanoid vasodilating substance. Without endothelium, a dilation was still observed and showed the persistence of an endothelium-independent component of flow-induced dilation in this preparation that remains to be determined.